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Biomedical subjects

H Wakasugi

Publications and source records attributed to H Wakasugi.

At least 127 records · Page 7Linked to original sources
PubMed1983

Leukemia cell lines can replace monocytes for mitogen-induced T-lymphocyte responses: this accessory function is dependent upon their differentiation stage.

Highly purified peripheral T lymphocytes do not proliferate in response to phytohemagglutinin A or concanavalin A, unless adherent HLA-DR+ monocytes are added as accessory cells. The accessory function (AF) of monocytes is mediated through the release of interleukin-1 (IL-1). We here report that cells from three human leukemic lines--K562, HL-60, and U-937--could exert AF and efficiently replace monocytes in a 72-hr mitogen-stimulated proliferation assay. This AF was clearly related to precise maturational stages of these cells, since the hematopoietic precursor K562 cells spontaneously exerted high AF but lost this property when treated with differentiation inducers such as sodium butyrate or phorbol 12-myristate 13-acetate (PMA). On the other hand, untreated HL-60 and U-937 cells exhibited no spontaneous AF, but they acquired this function when induced to differentiate either along the granulocytic pathway (dimethyl sulfoxide-treated HL-60 cells) or along the monocytic pathway (PMA-treated HL-60 and U-937 cells). Supernatants from PMA-triggered K562 or HL-60 cells allowed the proliferative response of murine thymocytes to phytohemagglutinin A and were therefore shown to contain IL-1. Analysis of phenotypical markers showed that AF and IL-1 production were not restricted to cells of the monocytic lineage. No HLA-DR antigen could be detected on K562 and HL-60 cells. Thus, the expression of HLA-DR antigens is not required for AF and IL-1 production in response to mitogens. Human leukemia cell lines could provide useful sources of human IL-1.

Cell Differentiation↗
PubMed1983

Evaluation of exocrine pancreatic function by oral administration of N-benzoyl-L-tyrosyl-p-aminobenzoic acid (PFD test) in primary diabetes mellitus.

Exocrine pancreatic function was evaluated in patients with primary diabetes mellitus by oral administration of N-benzoyl-L-tyrosyl-p-aminobenzoic acid (pancreatic function diagnostic test, PFD test) and p-aminobenzoic acid (PABA absorption test). In both primary diabetes mellitus and chronic pancreatitis, the mean excretion of PABA in the urine in the PFD test was significantly less than in the controls, and in 19 of 31 (61.3%) patients with primary diabetes mellitus and 11 of 12 (91.7%) patients with chronic pancreatitis there was a low PABA excretion rate. In contrast, the mean excretion of PABA in the urine in the PABA absorption test was significantly less in those with primary diabetes mellitus than in the controls. Therefore, to detect disturbances of pancreatic exocrine function in patients with primary diabetes mellitus, differences in the excretion of PABA in the urine between PFD test and PABA absorption test should be calculated. According to this method, the rate of abnormality was 12.9% in primary diabetes mellitus and 100% in chronic pancreatitis. There was a significant correlation between the excretion of PABA in the urine in the PFD test and results of renal function tests in primary diabetic patients with a normal range of serum creatinine levels. The serum PABA levels in the PFD test remained high in patients with primary diabetes mellitus and decreased in cases of chronic pancreatitis, as compared with the controls.

4-Aminobenzoic Acid↗
PubMed1983

Dynamic analysis of secretagogue-induced amylase secretion from rat pancreatic acini studied by perifusion system.

A perifusion system was applied for the study on stimulus-enzyme secretion coupling in dispersed pancreatic acini. The system is highly simple, preserves the acini up to more than 3 hr, and makes feasible clear-cut examination on the time course of enzyme secretion caused by secretagogues. Caerulein (10(-9) M) and carbamylcholine (10(-5) M) caused a biphasic amylase secretory pattern consisting of an initial burst secretion and a sustained one. Caerulein induced a persistent amylase release even after cessation of the stimulation, while carbamylcholine-stimulated amylase release returned to basal levels. Atropine inhibited completely carbamylcholine-stimulated amylase release and the successive stimulation by caerulein evoked the amylase secretion with a decreased initial burst secretion. In calcium free medium, caerulein and carbamylcholine induced only a slight secretion, particularly in the sustained secretion phase and a gradual increase occurred with the addition of calcium.

Amylases↗
PubMed1982

Calcium uptake into acini from rat pancreas: evidence for intracellular ATP-dependent calcium sequestration.

Intracellular ATP-dependent Ca2+-sequestration mechanisms were studied in isolated dispersed rat pancreatic acini following treatment with saponin or digitonin to disrupt their plasma membranes. In the presence of 45Ca2+ concentrations less than 10(-6) mol/liter, addition of 5 mmol/liter ATP caused a rapid increase in 45Ca2+ uptake exceeding the control by fivefold. ADP mimicked the ATP effect by 50 to 60%, whereas other nucleotides such as AMP-PNP, AMP-PCP, CTP, UTP, ITP, GTP, cAMP and cGMP did not. Maximal ATP-promoted Ca2+ uptake was obtained at 10(-5) mol/liter Ca2+. Inhibition of Ca2+ uptake by mitochondrial inhibitors was dependent on the Ca2+ concentration, indicating the presence of different Ca2+ storage systems. Whereas the apparent half-saturation constant found for mitochondrial Ca2+ uptake was approximately 4.5 X 10(-7) mol/liter, in the presence of antimycin and oligomycin (nonmitochondrial uptake) it was approximately 1.4 X 10(-8) mol/liter. In the absence of Mg2+ both ATP- and ADP-promoted Ca2+ uptake was nearly abolished. The Ca2+ ionophore and mersalyl blocked Ca2+ uptake, Electron microscopy showed electron-dense precipitates in the rough endoplasmic reticulum of saponin-treated cells in the presence of Ca2+, oxalate and ATP, which were absent in intact cells and in saponin-cells without ATP or pretreated with A23187. The data suggest the presence of mitochondrial and nonmitochondrial ATP-dependent C2+ storage systems in pancreatic acini. The latter is likely to be located in the rough endoplasmic reticulum.

Adenosine Diphosphate↗
PubMed1982

Plasma human pancreatic polypeptide response in chronic pancreatitis.

The changes of plasma pancreatic polypeptide (PP) and the relationship between PP response and exocrine pancreatic function in chronic pancreatitis are reported. In 260 healthy control subjects, plasma PP levels increased gradually with aging. Basal levels of PP in 30 patients with chronic pancreatitis were significantly lowered in comparison with age matched control subjects (control 95.0 +/- 10.3 pg/ml, chronic non-calcifying pancreatitis 45.0 +/- 7.3 pg/ml, chronic calcifying pancreatitis 40.4 +/- 6.0 pg/ml). Plasma PP response by insulin induced hypoglycemia, test meal ingestion, and pancreozymin-secretion represented a significant decrease in patients with chronic pancreatitis. Additionally, maximum PP response, especially in pancreozymin-secretin injection, had a good correlation with exocrine pancreatic function. These results suggest that the determination of plasma PP response is useful for the diagnosis of chronic pancreatitis.

Adult↗
PubMed1982

In vitro augmentation of human natural killer (NK) cell activity by a streptococcal preparation OK-432 and its extracts, protein M and polysaccharides.

Effect of a streptococcal preparation OK-432 and its derivatives on the augmentation of human natural killer cell activity in vitro was examined. The strong augmentation was found by the OK-432 stimulation. Cell separation procedures revealed that cytotoxic activity augmented by the stimulant was considered to be mediated mainly by nonadherent, nonphagocytic, IgG-Fc receptor positive, non-T cells, i.e. NK cells. In addition, supernates cultured with OK-432 augmented NK activity, suggesting some kinds of soluble factors released in the supernates may be participating on the augmentation of human NK activity by OK-432.

Antigens, Bacterial↗
PubMed1982

Potentiation of natural killer cell activity of human lymphocytes in vitro: the participation of interferon in stimulation with Staphylococcus aureus Cowan I bacteria but not with protein A.

In the previous paper we reported that human natural killer (NK) cell activity was augmented greatly by preincubation with Staphylococcus aureus Cowan I bacteria (SpA CoI) or its Protein A. We examined here whether the augmentation with these stimulants is ascribable to the direct activation of NK cells or mediated by some soluble factors produced by the stimulants. It was found that a significant amount of interferon (IFN) was produced by the SpA CoI-stimulation but not by the Protein A-stimulation, although the latter usually induced augmentation of NK-cell activity not less than SpA CoI-stimulation. IFN produced by SpA CoI was considered to belong to alpha-type IFN, because it was stable at pH 2.0 and could be neutralized effectively by anti-IFN alpha antibody. Kinetics of NK-cell activation by SpA CoI (but not by Protein A) were very similar to those by IFN alpha. Furthermore, augmentation of NK-cell activity with SpA CoI-stimulated supernatant was inhibited almost completely by diluted anti-IFN alpha antibody, whereas augmentation with Protein A-stimulated supernatant could not be abolished by the same treatment. It was, therefore, suggested that augmentation of NK-cell activity with SpA CoI might be ascribable in most part to the IFN induced, whereas Protein A can stimulated NK or T cells directly or soluble factors other than IFN might work as well.

Antibodies, Viral↗
PubMed1982

In vitro potentiation of human natural killer cell activity by a streptococcal preparation, OK-432: interferon and interleukin-2 participation in the stimulation with OK-432.

Inasmuch as human natural killer (NK) cell activity was markedly augmented by a streptococcal immunopotentiator, OK-432, both in vivo and in vitro, the mechanism in which OK-432 augmented human NK cell activity was analyzed. Culture supernatants of nonadherent lymphocytes stimulated with OK-432 significantly augmented NK cell activity. Significant activity of both interferon (IFN) (both alpha- and gamma-types) and interleukin-2 (IL-2) was detected in the culture supernatants from nonadherent lymphocytes. Concomitant treatment of supernatants with anti-IFN-alpha antiserum and pH-2 glycine-HCI buffer or the absorption of supernatants with an IL-2-dependent cell line completely abrogated the NK-augmenting activity, whereas the treatment with either one of these resulted in only partial elimination of the activity. These results indicate that OK-432 stimulates human nonadherent lymphocytes to produce IFN and IL-2 and that both factors are primarily responsible for the NK augmentation by OK-432.

Biological Products↗
PubMed1981

Analysis of Ca2+ fluxes and Ca2+ pools in pancreatic acini.

45Ca2+ movements have been analysed in dispersed acini prepared from rat pancreas in a quasi-steady state for 45Ca2+. Carbamyl choline (carbachol; Cch) caused a quick 45Ca2+ release that was followed by a slower 45Ca2+ 'reuptake'. Subsequent addition of atropine resulted in a further transient increase in cellular 45Ca2+. The data suggest the presence of a Cch-sensitive 'trigger' pool, which could be refilled by the antagonist, and one or more intracellular 'storage' pools. Intracellular Ca2+ sequestration was studied in isolated acini pretreated with saponin to disrupt their plasma membranes. In the presence of 45Ca2+ (1 microM), addition of ATP at 5 mM caused a rapid increase in 45Ca2+ uptake exceeding the control by fivefold. Maximal ATP-promoted Ca2+ uptake was obtained at 10 microM Ca2+ (half-maximal at 0.32 microM Ca2+). In the presence of mitochondrial inhibitors it was 0.1 microM (half-maximal at 0.014 microM). 45Ca2+ release could still be induced by Cch but the subsequent reuptake was missing. The latter was restored by ATP and atropine caused further 45Ca2+ uptake. Electron microscopy showed electron-dense precipitates in the rough endoplasmic reticulum of saponin-treated cells in the presence of Ca2+, oxalate and ATP which were absent in intact cells or cells pretreated with A23187. The data suggest the presence of a plasma membrane-bound Cch-sensitive 'trigger' Ca2+ pool and ATP-dependent Ca2+ storage systems in mitochondria and rough endoplasmic reticulum of pancreatic acini. It is assumed that Ca2+ is taken up into these pools after secretagogue-induced Ca2+ release.U

Adenosine Triphosphate↗
PubMed1981

Serum vitamin E, lipid peroxide and glutathione peroxidase in patients with chronic pancreatitis.

It has been reported that lipid peroxidation increases in patients with antioxidant deficiencies, such as vitamin E and glutathione peroxidase. The relationships between serum lipid peroxide and vitamin E on the one hand and glutathione peroxidase on the other were examined in 22 patients with chronic pancreatitis, often accompanied by malabsorption of fats and fat-soluble vitamins due to the impaired exocrine pancreatic function. Both serum vitamin E concentrations and glutathione peroxidase activities were depressed, especially in patients with chronic calcifying pancreatitis. On the other hand, serum lipid peroxide levels were elevated. A significant negative correlation was found between the serum lipid peroxide levels and vitamin E concentration. These findings suggest than an elevation of the serum lipid peroxide level may be due to the lack of an antioxidative defense mechanism, such as vitamin E, against lipid peroxide.

Chronic Disease↗
PubMed1981

Augmentation of natural killer (NK) cell activity by a streptococcal preparation, OK-432, in patients with malignant tumors.

Recently, a streptococcal preparation, OK-432 has been used successfully as an immunopotentiator for immunotherapy in patients with malignant tumors in Japan. In this paper, we report that the administration of OK-432 augments the cytotoxic activity of peripheral blood lymphoid cells against a natural killer (NK) cell-sensitive erythroleukemic cell line, K562, in tumor patients. In patients before or after surgery, sufficient amounts of OK-432 strongly augmented the cytotoxic activity within 3 days after the initial administration of OK-432. Thereafter the levels of cytotoxicity declined rapidly. The administration of a lower dose of OK-432 gave a lower increase in cytotoxicity. Enhanced cytotoxicity occurred with the reintroduction of OK-432 but remained at lower levels of activity. Characterization and fractionation of OK-432-induced effector cells revealed that the augmented cytotoxicity seemed to be carried mainly by NK cells. A low titer of interferon was detected in 3 of 10 patients within 72 hr after the first inoculation of the agent. Furthermore, we discuss the potency of OK-432 for the induction of interferon in detail.

Adjuvants, Immunologic↗
PubMed1981

Effect of La3+ on secretagogue-induced Ca2+ fluxes in rat isolated pancreatic acinar cells.

Addition of 0.1 mmol/l of La3+ to pancreatic acinar cells increased both the rate and extent of 45Ca+ uptake. Addition of 0.3 mmol/l La3+ did not change cellular 45Ca2+, whereas 1, 2, and 5 mmol/l gradually decreased it. If carbamylcholine (CCh) or the octapeptide of cholecystokinin-pancreozymin (CCK-OP) was added in the presence of low La3+ concentrations (0.1 and 0.3 mmol/l) to 45Ca2+-equilibrated cells, secretagogue-induced 45Ca2+ release-reuptake was not inhibited. At 1 and 2 mol/l of La3+, however, secretagogue-induced 45Ca2+ release was abolished, whereas uptake of 45Ca2+ was still increased by CCK-OP and CCh. At 5 mmol/l La3+, the effects of secretagogues were completely abolished. In the presence of 2 mmol/l La3+, the atropine-induced 45Ca2+ uptake in CCh-pretreated cells and the dibutyryl guanosine 3',5'-cyclic monophosphate-induced 45Ca2+ uptake in CCK-OP-pretreated cells were highly reduced. The data are interpreted to support our assumption that CCK-OP and CCh increase the plasma membrane permeability to Ca2+ in pancreatic acinar cells in addition to their action to initiate release of CA2+ from an intracellular Ca2+ trigger pool.

Animals↗